Basal levels of plasma homocyst(e)ine are frequently increased in patients with arterial occlusive diseases. Prospective and retrospective studies show that the presence of hyperhomocyst(e)inemia in such patients is independent of other conventional risk factors for atherosclerosis, although the associations between homocyst(e)ine and subclinical atherosclerosis seemed weaker after adjusting for certain risk factors. Moreover, genetic factors may be involved in the regulation of homocyst(e)inemia, as previously demonstrated. The negative correlation between plasma homocyst(e)ine and blood levels or intake of folate or Vitamins B12 and B6, as well as the effects of Vitamin replacement therapy suggest that nutritional components are also involved in the regulation of plasma homocyst(e)ine. Additionally, a number of physiologic conditions and pharmacological agents have been shown to modify homocyst(e)inemia. Even though the importance of homocyst(e)ine levels in arterial occlusive diseases and the influence of genetic, physiologic and pharmacological factors on the control of homocyst(e)ine levels are well-established, research on predictor variables for homocyst(e)inemia in subjects without arterial occlusive diseases should be expanded. Therefore, plasma homocyst(e)ine levels were determined in men who lack a history of atherosclerotic disease. Higher homocyst(e)ine concentrations were observed in hypertensive subjects than in normotensive subjects. Multivariate analyses demonstrated that systolic blood pressure, plasma uric acid and hematocrit were predictors of elevated plasma homocyst(e)ine after adjusting for other variables.